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Extracellular matrix regulates force transduction at VE-cadherin junctions.

Xinyu Kong1, Adrian Kapustka1, Brendan Sullivan1

  • 1Department of Biochemistry, University of Illinois at Urbana-Champaign, Urbana, IL 61801.

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Tugging on VE-cadherin activates integrins, reinforcing cell-cell junctions. This process involves key kinases and RhoA, showing how the extracellular matrix impacts cell adhesion and mechanical reinforcement.

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Area of Science:

  • Cell Biology
  • Biophysics
  • Mechanobiology

Background:

  • Intercellular mechanotransduction involves cell stiffening and cytoskeletal reinforcement.
  • VE-cadherin (VE-cad) complexes are crucial for cell-cell adhesion and force transmission.

Purpose of the Study:

  • To investigate the downstream effects of VE-cadherin tension on integrin activation.
  • To elucidate the role of integrins in reinforcing cadherin adhesions and intercellular force transduction.
  • To understand how extracellular matrix (ECM) composition influences this mechanotransduction pathway.

Main Methods:

  • Mechanical stimulation of VE-cadherin receptors.
  • Analysis of integrin activation and adhesion formation.
  • Identification of key signaling molecules (FAK, Abl, RhoA).
  • Assessment of ECM substrate effects (collagen, fibronectin) on VE-cad adhesions.

Main Results:

  • Tugging VE-cad initiates a cascade leading to integrin activation and new integrin adhesions.
  • Integrin activation recruits vinculin and actin, reinforcing VE-cad adhesions.
  • Focal adhesion kinase, Abl kinase, and RhoA GTPase are identified as key components in a positive feedback loop.
  • Integrin involvement sensitizes intercellular force transduction to the ECM by altering signal cascades, not junctional tension.
  • Specific integrins (α2β1, α5β1) differentially control actin remodeling based on ECM type (collagen, fibronectin).

Conclusions:

  • Integrins play a critical role in VE-cadherin force transduction, distinct from previously known antagonistic effects.
  • A novel mechanism is uncovered where ECM-dependent integrin signaling reinforces interendothelial cell-cell junctions.
  • This study highlights a previously unappreciated interaction between integrins, ECM, and cadherin-mediated adhesion reinforcement.